外周血多形核白细胞凋亡情况及生存率与急性胰腺炎严重程度相关性研究

目的研究急性胰腺炎大鼠模型外周血多形核白细胞即中性粒细胞(PMN)的凋亡情况及生存率与急性胰腺炎严重程度的关系。方法采用在大鼠胰胆管共同通道内逆行注射不同浓度的脱氧胆酸钠,制备不同严重程度的急性胰腺炎模型。18只SD大鼠随机分为对照组、模型1组(0.75%脱氧胆酸钠剂量组)、模型2组(1.5%脱氧胆酸钠剂量组)。分别于造模后6 h处死各组存活大鼠。观察各组大鼠的胰腺组织病理学变化、组织病理学评分,血清、腹水淀粉酶水平,腹水量及外周血清IL-6、IL-8水平。同时用TUNEL法分析外周血多形核白细胞凋亡情况,用流式细胞分析法分析外周血多形核白细胞存活率。并与急性胰腺炎严重程度各项指标进行统计学相关分析。结果模型1组大鼠较模型2组大鼠胰腺组织坏死及出血程度轻,组织病理学评分低,腹水及血清淀粉酶水平低,腹水量相对少,外周血清IL-6,IL-8水平低;病变程度较轻的模型1组大鼠外周血多形核白细胞凋亡指数比病变重的模型2组大鼠高(30±6 vs 20±4P<0.05);病变程度较轻的模型1组大鼠外周血多形核白细胞存活率比病变重的模型2组大鼠低[(56.12±4.21)%vs(67.15±5.11)%,P<0.05]。结论急性胰腺炎时,外周血多形核白细胞凋亡指数与急性胰腺炎严重程度呈负相关,外周血多形核白细胞存活率与急性胰腺炎严重程度呈正相关。     

中性粒细胞凋亡及caspase-3活性与多发伤患者MODS的关系

目的 研究外周血中性粒细胞凋亡及caspase-3的活性,探讨其在多发伤患者发生MODS中的意义.方法 选择多发伤患者55例,以是否发生MODS分为MODS组和非MODS组,采用流式细胞仪和TUNEL法定量检测外周血中性粒细胞的凋亡情况,流式细胞仪检测激活的caspase-3百分比,ELISA法检测血清IL-6,IL-10的水平.并分析中性粒细胞凋亡与IL-6和IL-10的相关性.结果 多发伤患者MODS组与非MODS组相比较,外周血中性粒细胞凋亡明显延迟,激活的caspase-3百分比明显降低(P<0.05).MODS患者血清IL-6水平增高,IL-10水平降低.MODS患者外周血中性粒细胞凋亡与其IL-6水平呈负相关,与IL-10水平呈正相关.结论 外周血中性粒细胞凋亡延迟,caspase-3活性下降,与多发伤患者发生MODS相关,IL-6和IL-10参与其调控.     

细胞因子白介素-6和白介素-10对中性粒细胞凋亡的影响

 目的观察白介素-6(IL-6)和白介素-10(IL-10)对离体健康人中性粒细胞凋亡的影响,了解它们在全身炎症反应综合征(Systemic inflammatory response syndrome,SIRS)和多器官功能障碍综合征(Multiple organ dysfunction syndrome,MODS)发病中的作用.方法选择20例健康志愿者,采取外周静脉血并分离中性粒细胞,每例分离的中性粒细胞平均分为4等份,分别给予生理盐水(对照组)、IL-6、IL-10、IL-6+IL-10,孵育24 h后,用AO/EB染色法计算每个样本中中性粒细胞的凋亡率、坏死率,并比较各组间凋亡率、坏死率的差异.结果与刘照组相比,IL-6组的中性粒细胞凋亡率显著降低(P＜0.01),L-10组中性粒细胞凋亡率则没有显著差异(P＞0.05);IL-10可对抗IL-6抑制中性粒细胞凋亡的作用(IL-6+IL-10组47.95±9.83 VS IL-6组35.80±8.59,P＜0.01).与对照组相比,IL-6组的中性粒细胞坏死率显著增加(P＜0.01),而IL-10组中性粒细胞坏死率则没有显著差异(P＞0.05).结论IL-6可抑制中性粒细胞的凋亡,增加中性粒细胞的坏死,促进中性粒细胞参与的炎症反应.IL-10不影响正常中性粒细胞的功能,但可抑制激活的中性粒细胞参与的炎症反应,具有一定的免疫调节作用.     

肾综合征出血热患者体内可溶型和膜型凋亡诱导配体的表达水平研究

目的:观察肾综合征出血热(HFRS)患者体内可溶型和膜型凋亡诱导配体的水平,探讨凋亡诱导配体与HFRS免疫病理损伤的关系。方法:应用夹心ELISA方法检测HFRS患者血浆中TNF-α、sFasL和sTRAIL的水平,同时利用流式细胞术检测膜型凋亡诱导配体在HFRS患者PBMC上的表达。结果:膜型凋亡诱导配体在健康对照的PBMC上几乎不表达,HFRS患者PBMC上TNF表达率为0.90%±0.05%;FasL的表达率为19.83±6.40%;TRAIL的表达率为15.79±4.73%。HFRS患者急性期血浆中的TNF-α(77.69±21.11pg/ml)、sFasL(40.69±6.75pg/ml)和sTRAIL(19.04±5.54pg/ml)水平分别是健康对照的4.8倍(16.26±14.09pg/ml)、6.0倍(6.76±1.01pg/ml)和1.8倍(10.72±1.41pg/ml)。结论:HFRS患者体内高表达的凋亡诱导配体可能与HTNV感染所致的免疫病理损伤有关。     

细胞因子及异丙酚对中性粒细胞内caspase-3活性的影响

 目的观察细胞因子白介素-6(IL-6)和白介素-10(IL-10)及异丙酚对离体的健康人中性粒细胞内caspase-3活性的影响,了解细胞因子及异丙酚影响中性粒细胞凋亡的机制.方法选择12例健康志愿者,采静脉血并分离中性粒细胞,将每例分离的中性粒细胞分为8组,分别加入生理盐水(对照组)、IL-6、IL-10、IL-6+IL-10、异丙酚、异丙酚的脂质溶剂intralipid、IL-6+异丙酚、IL-6+intralipid孵育,18 h后利用专用的试剂盒用流式细胞仪检测每个样本caspase-3激活的程度,并进行组间比较.结果与对照组相比,IL-6显著抑制中性粒细胞caspase-3的激活(P＜0.05),而IL-10、异丙酚和intralipid对caspase-3的激活则无显著影响;但IL-10和异丙酚均能够对抗IL-6对caspase-3激活的抑制(P＜0.05),intralipid则未表现对抗IL-6的作用.结论IL-6可抑制中性粒细胞内caspase-3的激活,而IL-10和异丙酚可对抗IL-6的这一作用,提示IL-6、IL-10和异丙酚对中性粒细胞凋亡的影响至少部分是通过影响caspase-3的激活来实现的.     

体外循环法对犬骨骼肌缺血再灌注损伤的保护作用

 目的 探讨体外循环法(extracorporeal circulation, ECC)对犬骨骼肌缺血再灌注损伤的保护作用。方法 首先建立犬骨骼肌缺血再灌注损伤模型,通过HE染色法观察组织炎性细胞浸润,利用TUNEL法观察组织凋亡的变化,特异性试剂盒检测LD、SOD等酶的变化,ELISA法检测IL-10和TNF-α等细胞因子的变化,评价ECC法再灌注模式对犬骨骼肌缺血再灌注损伤的保护作用。结果 模型组动物的组织炎性细胞浸润明显,诱导细胞凋亡发生,血清中LD[(2.6±0.3)mmol/ml vs.(5.2±0.1)mmol/ml ]、SOD[(15.2±1.2)U/ml vs.(31.1±2.1)U/ml]等酶的水平显著增加,同时血清中IL-10[(60.4±2.3)pg/ml vs.(89.2±1.5)pg/ml ]和TNF-α[(172.3±8.7)ng/l vs. (273.4±12.5 )ng/l]等细胞因子的含量显著增加 (P<0.01)。ECC法再灌注处理的动物,其组织炎性反应和细胞凋亡程度显著低于模型组动物,血清中上述酶和细胞因子的水平也显著降低,分别为:LD[(3.5±0.1)mmol/ml vs. (5.2±0.1) mmol/ml],SOD[(21.3±1.3)U/ml vs. (31.1±2.1) U/ml], IL-10[(69.4±2.6) pg/ml vs. (89.2±1.5)pg/ml]和TNF-α[(190.8±12.1)ng/l vs.(273.4±12.5)ng/l ](P<0.05)。结论 ECC法再灌注模式,对犬骨骼肌缺血再灌注损伤具有一定的保护作用。     

N-乙酰半胱氨酸对体外循环血清诱导的中性粒细胞-内皮细胞粘附的影响

目的观察N-乙酰半胱氨酸(NAC)对体外循环血清诱导的中性粒细胞-培养血管内皮细胞(PMN-EC)粘附的影响.方法本实验采用PMN-EC粘附模型,以体外循环血清致伤培养血管内皮细胞,及NAC处理,计数PMN-EC粘附率.结果体外循环前血清孵育内皮细胞,PMN-EC粘附率为(8.9±1.9)%,体外循环血清孵育内皮细胞,PMN-EC粘附率上升为(32.4±4.3)%,体外循环血清加入0.01、0.1、1、10mmol/L NAC时,PMN-EC粘附率分别降低至(30.5±4.7)%、(29.3±2.6)%、(21.6±3.7)%、(13±1.8)%.结论体外循环血清增加了培养血管内皮细胞对中性粒细胞的粘附能力,附加 NAC可明显抑制体外循环血清诱导的内皮细胞对中性粒细胞的粘附.     

Graves病131I治疗后血清sFas含量变化

目的　探讨Graves病 (GD) 1 31 I治疗前后血清可溶性细胞凋亡相关蛋白Fas(sFas)的变化特点及其临床意义。方法　用固相夹心法酶联免疫吸附试验 (ELISA)检测 6 1例GD患者1 31 I治疗前及治疗后不同时期血清sFas含量 ,并与对照组比较。结果　①GD患者sFas含量为 (174 8± 94 6 )pg ml,明显高于对照组 [(96 6± 10 2 )pg ml,P <0 0 1];与1 31 I治疗前组相比 ,缓解期组sFas含量 [(132 8±34 0 )pg ml]下降 ,但差异无显著性 (P >0 0 5 ) ,临床治愈组sFas含量 [(111 2± 13 2 )pg ml]进一步下降 ,差异有显著性 (P <0 0 5 ) ;甲状腺功能减退 (甲低 )组患者sFas含量 [(10 1 8± 16 3)pg ml]最低 ,差异有显著性 (P <0 0 1)。②sFas与GD患者甲状腺激素 (TH) ,包括TT3、TT4 、FT3和FT4 及促甲状腺激素受体抗体 (TRAb)呈正相关 (r=0 37～ 0 5 9,P <0 0 5 ) ,与年龄、促甲状腺激素 (TSH)、甲状腺球蛋白抗体 (TGAb)和甲状腺微粒体抗体 (TMAb)等无明显相关关系。结论　GD患者体内存在sFas异常表达 ,1 31 I治疗后不同时期内sFas含量呈规律性变化     

白细胞介素1β在131I治疗甲亢合并内分泌性眼病中的意义

目的 获得内分泌性眼病的自身免疫病理变化过程中机体的相关细胞因子白细胞介素113(IL-1β)表达痕迹的数据,探讨131I治疗甲亢后对合并内分泌性眼病患者外周血中IL-1β水平的影响.方法 采用前瞻性调查方法,选取内分泌性眼病患者31例,均有眼部症状和体征,血清甲状腺激素水平高于正常范围,并经眼眶CT检查排除其他疾病所导致的突眼,131I治疗剂量按照公式计算IL-1β的检测采用放射免疫分析法.结果 内分泌性眼病组较正常对照组血清IL-1β水平有不同程度升高:治疗前[(0.15±0.07)ng/ml]治疗后[(0.11±0.05)ng/ml]正常对照组[(0.10±0.03)ng/ml],H=68.088,P<0.001;131I治疗后较治疗前内分泌性眼病患者血清IL-1β水平亦有所下降(H=88.56,P<0.001);治疗后内分泌性眼病患者突眼度亦得到改善外周血中IL-1β水平与内分泌性眼病发病密切相关,并且内分泌性眼病患者经131I治疗后血清IL-1β水平较治疗前有所下降,突眼症状也明显改善.     

小儿传染性单核细胞增多症免疫状况动态观察

目的研究小儿传染性单核细胞增多症(IM)免疫功能动态变化,观察EB病毒(EBV)感染对免疫功能影响,为判断预后及治疗提供依据。方法应用流式细胞术对23例IM患儿急性期及恢复期外周血淋巴细胞CD3+、CD4+、CD8+、CD19+抗原进行检测,并与30例对照组健康儿童比较。结果IM患儿急性期外周血淋巴细胞CD3+、CD4+、CD8+、CD19+抗原分别为(80.74±8.51)%、(17.53±6.08)%、(57.38±14.90)%、(7.35±6.24)%,CD3+、CD8+显著高于对照组[(68.47±7.01)%、(24.10±4.65)%,P<0.01],CD4+、CD19+较对照组降低[(38.63±6.14)%、(19.00±5.27)%,P<0.01]。恢复期CD8+降低[(34.52±12.28)%],仍高于对照组(P<0.01);CD4+升高[(26.91±6.24)%],仍低于对照组(P<0.01)。结论IM患儿急性期外周血淋巴细胞亚群显著异常,恢复期机体仍处于免疫紊乱状态,CD4+T细胞持续低下可能需免疫调节治疗。     

早期强化胰岛素治疗对重症脓毒症患者炎性因子及免疫功能的影响

目的探讨早期强化胰岛素治疗对重症脓毒症患者血清IL-6及外周血单核细胞mCD14、HLA-DR表达的影响。方法选择重症脓毒症患者50例,随机分为强化组和常规组,选择健康人群30例为对照组,ELISA方法检测血清IL-6的浓度,流氏细胞术检测单核细胞mCD14、HLA-DR表达,同时记录ApachⅡ评分和死亡率。结果强化组治疗后血清IL-6水平、ApachⅡ评分及死亡率均明显降低,单核细胞mCD14、HLA-DR表达率较常规组明显升高。结论早期强化胰岛素治疗可以更好地抑制机体的炎性反应,改善免疫功能,提高生存率,改善预后。     

大鼠颅脑外伤后早期脑微血管内皮细胞功能和结构的改变

目的 通过对大鼠脑损伤后早期脑血管内皮细胞的功能和结构的观察,探讨脑外伤早期微循环障碍形成的发生机制.方法 用改良Marmarous法建立大鼠闭合性脑损伤动物模型,伤后1 h、4 h、8 h、12 h、24 h、3 d及7 d分别自损伤组和假手术对照组取10只大鼠取脑,5只行免疫组化、5只行荧光定量PCR测定脑血管内皮细胞活化标志物假性血管性血友病因子(vWF)和血栓调节蛋白(TM)的表达变化.结果 大鼠脑损伤后TM和vWF在4 h开始表达,24 h达到峰值,7 d恢复正常.假手术对照组各时段TM和vWF的表达水平与损伤组比较,差异有统计学意义(P<0.05).结论 脑损伤早期脑微血管内皮细胞的活化是早期继发性脑损伤形成的重要机制.     

Anti-inflammatory effect of low-dose X-irradiation and the involvement of a TGF-beta1-induced down-regulation of leukocyte/endothelial cell adhesion

PURPOSE: Low-dose radiotherapy (LD-RT) is known to exert an anti-inflammatory effect, but the underlying radiobiological and immunological mechanisms remain elusive. In recent studies, we observed a reduced adhesion of peripheral blood mononuclear cells (PBMC) to endothelial cells (EC) after LD-RT (0.3-0.7 Gy). This shows that this treatment affects the initial steps of the inflammatory response. To explore the role of inflammatory mediators in this process, we investigated the expression of Transforming growth factor beta(1) (TGF-beta(1)) and Interleukin 6 (IL-6) after LD-RT. MATERIALS AND METHODS: EC were grown to subconfluence and irradiated with single-dose LD-RT. Twenty-hours after irradiation, EC were treated with IL-1beta for 4 h and then incubated with peripheral blood mononuclear cells (PBMC). Adherent PBMC were counted when using light microscopy. Expression of the cytokines TGF-beta(1) and IL-6 was measured by ELISA, and mRNA levels were analysed by the RNAse-protection assay (RPA). Surface expression of E-selectin was quantified by flow cytometry. RESULTS: A relative minimum of adhesion was observed after LD-RT between 0.3 and 0.7 Gy. This was paralleled by an expression maximum of TGF-beta(1) and IL-6, as shown by protein and mRNA levels, respectively. Neutralization of TGF-beta(1) by monoclonal antibodies, but not of IL-6, increased PBMC adhesion to EC nearly to control levels. In addition, fluorescence activated cell sorter (FACS) analysis of irradiated EC demonstrated a down-regulation of E-selectin in the same dose range. CONCLUSION: Low-dose X-irradiation between 0.3 and 0.7 Gy induced a relative maximum of TGF-beta(1) production by stimulated EC. This results in a down-regulation of leukocyte/PBMC adhesion and may contribute to the anti-inflammatory effect of LD-RT.     

急性胰腺炎患者外周血中Th17和Treg细胞及其细胞因子水平变化

目的：研究急性胰腺炎患者外周血中辅助性T细胞(Th17细胞)与调节性T细胞（regulatory cells,Treg细胞）及其细胞因子的水平变化。方法选取2014年8月—2015年8月来我院接受治疗的急性胰腺炎患者92例,其中轻度急性胰腺炎（mild acute pancreatitis,MAP）患者39例作为MAP组,中度急性胰腺炎（moderately severe acute pancreatitis,MSAP）患者29例作为MSAP组,重度急性胰腺炎（severe acute pancreatitis,SAP）患者24例作为SAP组,并以25名健康体检者作为对照组。采用流式细胞术分别检测4组外周血中Th17和Treg细胞比例,采用实时荧光定量PCR分析外周血白细胞中白介素17（IL-17）、白介素6（IL-6）、白介素10（IL-10）、转化生长因子-β（TGF-β）等因子mRNA水平,采用ELISA法检测血清中细胞因子IL-17、IL-6、IL-10、TGF-β等因子蛋白质水平。结果与对照组比较,MAP、MSAP和SAP组外周血Treg细胞比例、Treg/Th17比值明显下降,而Th17细胞比例明显升高（P＜0.05）。与对照组比较,MAP、MSAP和SAP组患者外周血细胞和血清中IL-10和TGF-β mRNA和蛋白质水平显著下降（P＜0.05),而IL-17和IL-6 mRNA和蛋白质水平显著升高（P＜0.05）。结论急性胰腺炎患者外周血Treg细胞和Th17细胞比例以及相关细胞因子表达水平失衡,对进一步探讨急性胰腺炎发病机制具有重要意义。     

Anti-inflammatory effect of low-dose X-irradiation and the involvement of a TGF-β 1 -induced down-regulation of leukocyte/endothelial cell adhesion

Purpose : Low-dose radiotherapy (LD-RT) is known to exert an anti-inflammatory effect, but the underlying radiobiological and immunological mechanisms remain elusive. In recent studies, we observed a reduced adhesion of peripheral blood mononuclear cells (PBMC) to endothelial cells (EC) after LD-RT (0.3-0.7 Gy). This shows that this treatment affects the initial steps of the inflammatory response. To explore the role of inflammatory mediators in this process, we investigated the expression of Transforming growth factor β 1 (TGF- β 1) and Interleukin 6 (IL-6) after LD-RT. Materials and Methods : EC were grown to subconfluence and irradiated with single-dose LD-RT. Twenty-hours after irradiation, EC were treated with IL-1 β for 4 h and then incubated with peripheral blood mononuclear cells (PBMC). Adherent PBMC were counted when using light microscopy. Expression of the cytokines TGF- β 1 and IL-6 was measured by ELISA, and mRNA levels were analysed by the RNAse-protection assay (RPA). Surface expression of E-selectin was quantified by flow cytometry. Results : A relative minimum of adhesion was observed after LD-RT between 0.3 and 0.7 Gy. This was paralleled by an expression maximum of TGF- β 1 and IL-6, as shown by protein and mRNA levels, respectively. Neutralization of TGF- β 1 by monoclonal antibodies, but not of IL-6, increased PBMC adhesion to EC nearly to control levels. In addition, fluorescence activated cell sorter (FACS) analysis of irradiated EC demonstrated a down-regulation of E-selectin in the same dose range. Conclusion : Low-dose X-irradiation between 0.3 and 0.7 Gy induced a relative maximum of TGF- β 1 production by stimulated EC. This results in a down-regulation of leukocyte/PBMC adhesion and may contribute to the anti-inflammatory effect of LD-RT.     

Impact of a competitive marathon race on systemic cytokine and neutrophil responses

PURPOSE: To investigate whether cytokines and neutrophils mediate exercise-related pathogenesis, we examined their responses and possible association after exhaustive exercise. METHODS: Plasma and urine samples were obtained from 10 male runners before and after a 42.195-km marathon race. Major cytokines and neutrophil activation markers [myeloperoxidase (MPO) and lactoferrin (LTF)] were measured by enzyme-linked immunosorbent assays. Functional modulation of standard neutrophils and monocytes by plasma was determined on their luminol-dependent chemiluminescence responses. RESULTS: The race induced peripheral neutrophilia accompanied by an increase in band neutrophils and monocytosis. Plasma MPO and LTF concentrations increased significantly by 1.8 and 1.4 times after the race. There was a greater increase in urine concentrations of MPO and LTF, 12.3 and 3.5 times after exercise, respectively, suggesting that neutrophil activation occurred and that renal clearance exceeded the increase in plasma concentrations. Plasma interleukin (IL)-6, IL-8, IL-10, granulocyte colony-stimulating factor (G-CSF), macrophage CSF (M-CSF), and monocyte chemotactic protein 1 (MCP-1) increased significantly after the race, and urine IL-1beta, IL-6, G-CSF, M-CSF, and MCP-1 increased significantly. The plasma IL-6 responses correlated with the increases of band neutrophil count (r = 0.860, P < 0.01), suggesting IL-6-mediated bone marrow release of neutrophils. Furthermore, the increases in urine MPO concentration were correlated with increases in urine IL-6 (r = 0.868, P < 0.01) and G-CSF (r = 0.875, P < 0.01), suggesting that these cytokines promoted neutrophil activation. However, preincubation of neutrophils and monocytes with postexercise plasma could not cause priming responses, possibly because of the exercise-induced enhancement of plasma antioxidant activity. CONCLUSION: Although many cytokines recruiting and priming neutrophils and monocytes were secreted and functional after exhaustive exercise, overwhelming antioxidant and antiinflammatory defenses were induced, preventing exercise-induced oxidative stress.     

经颈静脉肝内门腔静脉分流术中胆汁漏出对内皮细胞生长及功能的影响

目的 探讨胆汁对离体培养的内皮细胞生长及功能的影响，进一步了解胆汁对支架内皮化的影响。方法 取人脐静脉内皮细胞进行体外培养，分别加入5％、10％、15％、20％、25％胆汁干预，观察内皮细胞生长状况，收获的细胞测总蛋白，四唑盐（MTT）吸光度值，条件培养液测血管性假性血友病因子（von Willebrand factor，简称vWF)行内皮细胞鉴定及功能测定。结果 含5％、10％、15％胆汁的细胞生长状况与不含胆汁者相似，含20％、25％胆汁的细胞明显减少并显幼稚；含25％胆汁的细胞MTT吸光度值及总蛋白较无胆汁者降低，差异有非常显著性意义（Kruskal-Wallis秩和检验，χ^2=29.913,P=0.0009及χ^2=18.857,P=0.002)；含20％以上浓度胆汁的细胞条件培养液中vWF含量也明显降低，差异有非常显著性意义（Kruskal-Wallis秩和检验，χ^2=27.213,P=0.0001)。所收获的细胞vWF测定均阳性。结论 一定浓度的胆汁具有抑制内皮细胞的生长及分泌vWF的功能。所收获的细胞vWF测定均阳性。结论 一定浓度的胆汁具有抑制内皮细胞的生长及分泌vWF的功能。     

原代白血病细胞IL-6受体α表达的实验研究

目的：分析不同类型原代白血病细胞IL-6R基因及IL-6R蛋白的表达情况。方法：采用RT-PCR方法对取自29例白血病患者的原代白血病细胞和8例健康人外周血单个核细胞的IL-6R基因表达情况进行了分析，并应用原位杂交技术和免疫组织化学方法对细胞表面的IL-6受体蛋白进行了检测。结果：20例急性髓细胞白血病均明显表达IL-6R mRNA；9例急性淋巴细胞白血病中有2例为阳性，其余7例为阴性；8例正常人PBMC中6例阴性。2例有弱表达。免疫组化和原位杂交结果与RT-PCR实验结果相一致。结论：IL-6R可作为急性髓系白血病免疫治疗的候选靶位点。     

慢性阻塞性肺病C-反应蛋白与内皮促凝血活化因子变化研究

目的 探讨慢性阻塞性肺疾病(COPD)急性加重期患者血清C-反应蛋白(C-reactive protein,CRP)、血管性血友病因子抗原(von Willebrand factor antigen,vWF:Ag)、凝血因子Ⅰ即纤维蛋白原(fibrinogen,Fbg)、抗凝血酶(antithrombin,AT)-Ⅲ,D-二聚体的含量、活性的变化及其临床意义.方法 检测40例COPD患者急性加重期、稳定期及20例健康体检者(对照组)血清CRP、内皮细胞活化产物vWF:AS、凝血因子Fbg、抗凝因子AT-Ⅲ、纤维蛋白降解产物D-二聚体的含量,同时进行肺功能和动脉血气测定.结果 COPD患者急性加重期血清CRP、vWF:Ag、Fbg、D-二聚体水平较稳定期及对照组均明显升高,稳定期水平较对照组明显升高,差异有统计学意义(P<0.05或P<0.01);COPD患者血清CRP、vWF:Ag、Fbg及D-二聚体水平与第1秒用力呼气容积与用力肺活量的比值(FEV_1/FVC)呈负相关,而CRP与各个促凝指标呈正相关;AT-Ⅲ各组间差异无统计学意义(P>0.05).结论 COPD急性加重期的系统性炎症反应与内皮-促凝系统的激活有关,监测CRP、vWF:Ag、Fbg、D-二聚体表达对患者病情、疗效判断,预测预后及指导临床用药有一定价值.     

尖锐湿疣患者中趋化因子受体CXCR1、CXCR4及其配体的水平

目的：测定趋化因子受体CXCR1与CXCR4及其配体在尖锐湿疣（CA）患者中的水平。方法：病程大于3个月的CA患者30例,实时定量PCR法检测外周血单个核细胞（PBMC）及皮损中CXCR1与CXCR4mRNA表达水平,流式细胞仪分析外周血白细胞CXCR1与CXCR4的表达情况,ELISA检测血清IL-8与SDF-1α的水平;设30例健康人为正常对照。结果：CX-CR4 mRNA与SDF-1α在CA患者中的水平显著高于对照组（均P〈0.01）。结论：CXCR4与SDF-1α可能参与了CA的发病机制。